首页|慢性应激通过局灶性黏附途径促进颈动脉粥样硬化进展

慢性应激通过局灶性黏附途径促进颈动脉粥样硬化进展

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目的 验证慢性应激在颈动脉粥样硬化发生发展中的可能机制.方法 本研究采用以小鼠构建慢性应激动物模型和动脉粥样硬化动物模型.通过蛋白质印迹实验研究局灶性黏附通路的作用.最后采用生物信息学方法在公共数据库验证通路.结果 构建并评估慢性应激小鼠模型和动脉粥样硬化小鼠模型,采用蛋白质印迹显示动脉粥样硬化小鼠模型中局灶性黏附通路关键因子表达降低,在慢性应激合并动脉粥样硬化的小鼠模型中该通路关键因子进一步下调,同时伴随炎症因子升高.以生物信息方法鉴定差异表达基因,并富集到局灶性黏附通路.蛋白质互作网络分析显示此通路中核心基因FLNA、MYH9与颈动脉粥样硬化相关.结论 在慢性应激中,局灶性黏附通路在促进动脉粥样硬化的发展中起到关键作用,MYH9和FLNA被确定为该过程中潜在的核心基因.
Chronic Stress Promotes the Progression of Carotid Atherosclerosis through Focal Adhesion Pathway:Evidence from Mouse Models
Objective To verify the possible mechanism of chronic stress in the occurrence and development of carotid atherosclerosis.Methods C57BL/6J and Apoe-/-mice were divided into normal control,chronic stress,atherosclerosis and atherosclerosis+chronic stress groups.Study the role of focal adhesion pathway through protein blotting experiments.Finally,bioinformatics methods were used to validate pathways in public databases.Results The chronic stress(CS)mice model and atherosclerosis(AS)mice model were constructed and evaluated.Western blotting showed that the expression of Focal adhesion pathway protein in AS mice was reduced,and that in CS+AS mice,the expression of Focal adhesion pathway protein was further reduced,accompanied by increased inflammatory factors.Identify differentially expressed genes using bioinformatics methods and enrich them into the Focal adhesion pathway.Protein interaction network(PPI)analysis showed that the core genes FLNA and MYH9 in this pathway were associated with carotid atherosclerosis.Conclusion In chronic stress,focal adhesion pathway plays a key role in promoting the development of atherosclerosis.MYH9 and FLNA have been identified as potential key genes in this process.

Chronic stressCarotid atherosclerosisBioinformaticsFocal adhesion pathway

陈雷、高尚、邓鸿儒、孟令丙、李拥军

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首都医科大学附属复兴医院血管外科,北京 100038

中国医学科学院北京协和医学院,北京 100730

北京医院血管外科,国家老年医学中心,中国医学科学院老年医学研究所,北京 100730

清华大学临床医学院附属北京清华长庚医院心内科,北京 102218

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慢性应激 颈动脉粥样硬化 生物信息学 局灶性黏附

2024

中国分子心脏病学杂志
中国医学科学院,中国协和医学院

中国分子心脏病学杂志

CSTPCD
影响因子:0.426
ISSN:1671-6272
年,卷(期):2024.24(1)
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